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PubMed1995

Metabolism of cholesterol and low- and high-density lipoproteins in primary biliary cirrhosis: cholesterol absorption and synthesis related to lipoprotein levels and their kinetics.

Cholesterol absorption, elimination, and synthesis, and low-density lipoprotein (LDL) and high density lipoprotein (HDL) kinetics were studied in patients with mild to severe primary biliary cirrhosis (PBC) (n = 16) to show how this cholestatic disease modified cholesterol and lipoprotein metabolism as compared with healthy controls (n = 50). Serum total and lipoprotein cholesterol and triglyceride levels were similar in the two groups, but in PBC, especially in severe forms, very low density lipoprotein (VLDL) was rich in apoprotein (apo) B and cholesterol and low in triglycerides, whereas LDL was rich in triglycerides and low in esterified cholesterol, and HDL was enriched by surface lipids, phospholipids, and free cholesterol. In severe PBC, the fractional catabolic rate (FCR) for LDL apo B was reduced. The transport rate (TR) for LDL apo B was unaffected and it tended to correlate with the LDL apo B and LDL cholesterol levels in PBC, whereas in the controls the LDL apo B concentration was regulated by both the FCR and TR, and LDL cholesterol was regulated only by FCR. FCR for apo A-I in HDL was unaltered in PBC, but TR for apo A-I was reduced in the severe cases. Cholesterol absorption efficiency was significantly reduced in PBC (14.5 +/- 3.0% in severe PBC and 34.0 +/- 2.5% in mild PBC vs. 47.4 +/- 1.4% in the controls, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1995

High lipid levels in very low density lipoprotein and intermediate density lipoprotein may cause proteinuria and glomerulosclerosis in aging female analbuminemic rats.

BACKGROUND: Male rats are generally more prone to developing renal disease than female rats. However, female Nagase analbuminemic rats (NAR) are profoundly hyperlipidemic and develop proteinuria and glomerulosclerosis after uninephrectomy. Male NAR are less hyperlipidemic and are resistant to developing renal damage after uninephrectomy. Ovariectomy markedly decreases hepatic triglyceride secretion and plasma triglyceride levels in the female NAR. EXPERIMENTAL DESIGN: In this study, we investigated the relationship between plasma lipids and lipoprotein composition as well as the development of proteinuria, glomerular apolipoprotein and lipid deposition, and glomerulosclerosis in aging female and male analbuminemic rats. We also studied whether ovariectomy in female NAR at an early age would protect their renal function in old age. RESULTS: Aging hyperlipidemic female NAR with high triglyceride and cholesterol levels in very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) were found to develop spontaneous proteinuria at 9 months of age. Glomerular lipid deposition and glomerulosclerosis were observed at 18 months of age. In male NAR that had lower lipid levels in VLDL and IDL, only mild proteinuria and no glomerular lipid deposition or glomerulosclerosis were observed up to the age of 22 months. Concurrently ovariectomized NAR demonstrated profound and persistent decreases in triglyceride and cholesterol content of VLDL and IDL as well as total plasma triglycerides, without much change in LDL, high density lipoprotein, total plasma cholesterol, or apolipoprotein B, and they remained completely free of proteinuria and glomerulosclerosis. Apolipoprotein B deposition in glomeruli was not different in the oldest female, male, or ovariectomized NAR. No important differences were observed in glomerular diameter between the three different groups up to the age of 1 year. CONCLUSIONS: These findings point to an important role of elevated lipid content of the triglyceride-rich lipoproteins VLDL and IDL in the pathogenesis of proteinuria and glomerulosclerosis in the female NAR.

Aging↗
PubMed1981

Changes in high density lipoprotein subfractions and other lipoproteins by exercise.

Seventeen previously sedentary men (aged 30-45) were exercised approximately twice weekly over a 10-week period during which time there was a significant fall in low density lipoprotein cholesterol, but total high density lipoprotein (HDL) did not change. The subfraction HDL2 showed an initial fall at two weeks of training with a subsequent rise above the baseline by 10 weeks. HDL3 cholesterol tended to change in an opposite direction to HDL2 thus accounting for no significant change in total HDL cholesterol. Smoking or drinking habits did not change throughout the study. As body weights did not change significantly through the study, energy intake must have increased with probable increased very low density lipoprotein (VLDL) production. Loss of apoprotein C-peptides from HDL2 associated with activation of lipoprotein lipase, and clearance of VLDL, could have caused redistribution of C-apoproteins between HDL3 leading to the changes seen, with the establishment of a new equilibrium with continued training by 10 weeks.

Adult↗
PubMed2001

Direct measurement of low-density-lipoprotein cholesterol is more effective than total cholesterol for the purpose of lipoprotein screening.

BACKGROUND: We have developed a new method for chemically measuring blood low-density-lipoprotein (LDL) cholesterol. In the present study, we simulated guidelines of the National Cholesterol Education Program (NCEP) using our LDL cholesterol measurements. METHODS: Blood samples were collected from 1,069 individuals (519 males, 550 females) who were referred to our laboratory at Niigata University Hospital for lipoprotein analysis. LDL cholesterol levels were determined according to our assay protocol, which has been published previously. Subjects were categorized by NCEP guidelines and identified "false positives" and "false negatives" on the basis of LDL cholesterol levels measured by our method. RESULTS: The sensitivity of the NCEP guidelines is 87.5% and the specificity is 87.1%, provided we assume that every individual has fewer than two risk factors for coronary heart disease. If we assume that every individual has two or more risk factors, the sensitivity and specificity of the guidelines are 99 and 56.8%, respectively. CONCLUSION: This study presents an opportunity to reevaluate guidelines for routine lipoprotein screening. The chance that individuals with higher LDL cholesterol and lower high-density-lipoprotein cholesterol levels in serum would be missed at initial classification should be zero. The chance that individuals with desirable lipid levels would undergo further lipoprotein analysis should be decreased. Since the new method can be implemented cost-effectively in routine lipoprotein screening, direct measurement of LDL cholesterol could replace total cholesterol.

Adult↗
PubMed1987

Interdependence of associations of physical activity, smoking, and alcohol and coffee consumption with serum high-density lipoprotein and non-high-density lipoprotein cholesterol--a population study in eastern Finland.

The interdependence of the associations of physical activity, smoking, and consumption of alcohol and coffee with serum high-density lipoprotein and non-high-density lipoprotein cholesterol concentrations was studied in 9,347 persons ages 25-64 years from east and southwest Finland. In covariance analyses with corrections for age, body mass index, saturated fat index, and fasting time, the mean adjusted serum high-density lipoprotein to non-high-density lipoprotein cholesterol ratio was high among physically active male non-smokers but not among smokers (P = 0.024 for two-way interaction). The cholesterol ratio was lower among both men (P = 0.010 for two-way interaction) and women (P = 0.030 for two-way interaction) reporting no or very little use of alcohol, and this association was stronger among smokers and women with high coffee consumption (P less than 0.001 for two-way interaction). Our data suggest that the elevating effect of regular physical exercise on serum high-density lipoprotein cholesterol may be absent in smokers, whereas that of alcohol is greater in smokers than nonsmokers. High coffee consumption associates with decreased serum high-density lipoprotein cholesterol levels in smokers but increased levels in non-smokers.

Adult↗
PubMed2001

Correlation between total homocysteine, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol in the serum of patients with myocardial infarction.

OBJECTIVES: Determine the Low-density lipoprotein cholesterol (LDL-C), High-density lipoprotein cholesterol (HDL-C) and serum total homocysteine in myocardial infarction patients and control subjects. DESIGN AND METHODS: The study group consisted of 126 patients 67 male, and 59 females, aged 29-73 (mean 48.65 +/- 3.81) years. The entry criteria for the patient group was typical or atypical chest pain, unequivocal changes in the electrocardiogram. The control group consisted of 135 normal volunteers, 71 male and 64 females, age 21-63 (mean 42.73 +/- 5.79) years. Measurement of serum total homocysteine was performed using gas chromatography. Measurement of Low-density lipoprotein cholesterol, and High-density lipoprotein cholesterol were performed using spectrophotometer. RESULTS: Patients with myocardial infarction were found to have higher serum total homocysteine levels than controls, (P < 0.05). Serum total homocysteine levels were significantly correlated with low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. There was a negative correlation between total homocysteine and HDL-C levels (P < 0.05, r = -0.93). There was a positive correlation between total homocysteine and LDL-C levels (P < 0.05, r = 0.98). CONCLUSIONS: The above mentioned findings suggest the potential usefulness of LDL-C, HDL-C and serum total homocysteine as prognostic markers in myocardial infarction patients. These findings should influence future studies on the etiology and pathogenesis of myocardial infarction.

Adult↗
PubMed2000

Overexpression of low density lipoprotein receptor eliminates apolipoprotein B100-containing lipoproteins from circulation and markedly prevents early atherogenesis in apolipoprotein E-deficient mice.

Apolipoprotein E (ApoE) plays a pivotal role in the metabolism of apolipoprotein B (apoB)-containing lipoproteins. The defective apoE gene in humans can cause elevated plasma levels of apoB-containing lipoproteins such as chylomicron remnant and intermediate density lipoprotein (IDL). In this study, we examined whether liver-selective high-level expression of low-density lipoprotein receptor (LDLR) could affect the lipoprotein profile and atherogenesis in apoE-deficient (apoE-/-) mice. ApoE knockout mice expressing LDLR transgene in liver [apoE-/-;Tg(LDLR+/-)] were prepared after mating apoE-/- mice with the human LDLR transgenic mice. The apoE-/-;Tg(LDLR+/-) and littermate apoE-/- mice were fed a normal diet and sacrificed at 18 weeks of age. (1) The plasma levels of cholesterol and triglyceride in apoE-/-;Tg(LDLR+/-) mice were 51 and 33% lower than those of apoE-/- mice, respectively. (2) In the plasma of apoE-/-;Tg(LDLR+/-) mice, the levels of apoB-containing lipoprotein were reduced and apoB100-containg particles were totally eliminated. (3) By histochemical analysis, apoE-/-;Tg(LDLR+/-) mice showed drastic suppression of early atherogenesis; the lesion area of these mice was 1/70 of that in the littermate apoE-/- mice. These results indicate that, even in apoE-defective subjects, induction of hepatic LDLR expression could protect from early atherogenesis.

Animals↗
PubMed2006

Modified low-density lipoproteins and high-density lipoproteins. From investigation tools to real in vivo players.

It has long been known that the oxidative state of the various plasma lipoproteins modulates platelet aggregability, thereby contributing to atherogenesis. Low-density lipoprotein (LDL), occurring in vivo both in the native and oxidised forms, interacts directly with platelets, by binding to specific receptors. While the identity of the receptors for native LDL and some subfractions of high-density lipoproteins (HDL) remains disputed, apoE-containing HDL(2) binds to LRP8. The nature of these interactions as well as the distinction between candidate receptor proteins was elucidated using covalently modified apolipoproteins, which pointed to the participation of apolipoproteins in high affinity binding. However, the platelet effects initiated by binding of native lipoproteins remain controversial. Some of this ambiguity can be traced to the fact that native LDL inevitably undergoes substantial oxidisation upon modification, including by radiolabelling. The platelet-activating effects provoked by oxidised LDL are irrefutable, but many details remain unknown. The role of CD36 in platelet binding by oxidised LDL is well established, although additional receptors may exist. Much less is known about the interaction of oxidised HDL with platelets, since platelet activation was observed in some, but not all studies. Various frequently applied in vitro oxidation methods produce modified lipoprotein species that may not be relevant in vivo. Based on the reported modifications obtained by in vitro oxidation of LDL, early investigations focused mainly on the formation and the eventual effects of oxidised lipids. More recently, alterations to lipoproteins performed using hypochloric acid and myeloperoxidase redirected the attention to the role of modified apoproteins in triggering platelet responses.

Apoproteins↗
PubMed2001

Genetic diagnosis of familial hypercholesterolemia in a South European outbreed population: influence of low-density lipoprotein (LDL) receptor gene mutations on treatment response to simvastatin in total, LDL, and high-density lipoprotein cholesterol.

The aims of this study were to examine the presence of mutations in the low-density lipoprotein receptor gene among subjects clinically diagnosed with familial hypercholesterolemia and to analyze whether the molecular diagnosis helps to predict the response to simvastatin treatment in our familial hypercholesterolemia population. Fifty-five probands and 128 related subjects with familial hypercholesterolemia were studied. Genetic diagnosis was carried out following a three-step protocol based on Southern blot and PCR-single strand conformational polymorphism analysis. A randomized clinical trial with simvastatin was conducted in 42 genetically diagnosed subjects with familial hypercholesterolemia classified as carriers of null mutations (n = 22) and of defective mutations (n = 20). A mutation-causing familial hypercholesterolemia was identified in 46 probands (84%). In 41 of them (89%), a total of 28 point mutations were detected, 13 of which have not been previously described. The remaining five probands (11%) were carriers of large rearrangements. Familial hypercholesterolemia with null mutations showed a poor response to simvastatin treatment. The mean percentage reduction of plasma total and low-density lipoprotein cholesterol levels in these subjects were significantly lower (24.8 +/- 10.3 vs. 34.8 +/- 10.9, P = 0.04 and 30.0 +/- 39.8 vs. 46.1 +/- 18.2, P = 0.02, respectively) than in subjects with defective mutations. Baseline and posttreatment high-density lipoprotein cholesterol plasma values were significantly lower in subjects with familial hypercholesterolemia with null mutations (P < 0.001). In an outbreed Caucasian population, a three-step protocol for genetic screening detected a mutation in the low-density lipoprotein receptor gene in a high percentage (84%) of subjects with familial hypercholesterolemia. Subjects with familial hypercholesterolemia with null mutations (class I) showed lower plasma high-density lipoprotein cholesterol values and a poor low-density lipoprotein cholesterol response to simvastatin treatment.

Adult↗
PubMed1996

Low-density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor on murine peritoneal macrophages mediates the binding and catabolism of low-density lipoprotein.

Low-density lipoprotein receptor-related protein (LRP)/alpha 2-macroglobulin receptor is a member of the low-density lipoprotein receptor family. It is known to bind a wide variety of unrelated ligands including alpha 2-macroglobulin-proteinase complexes, tissue plasminogen activator, apolipoprotein E-enriched very low density lipoprotein, lipoprotein lipase, and Pseudomonas exotoxin A. Receptor-associated protein (RAP), a protein which copurifies with LRP, can inhibit the binding and internalization of all known ligands to LRP. Recent studies have shown that some ligands can bind to more than one receptor in this family. However, the ability of low-density lipoprotein (LDL) to bind to LRP in addition to the LDL receptor has not been demonstrated consistently. In this study we demonstrate that LDL binds with high affinity to macrophage cell surface receptors at 4 degrees C (Kd = 1.8 nM) and competes for the binding of a receptor-recognized form of alpha 2-macroglobulin (alpha 2M*) (Ki = 3 nM). alpha 2M* and RAP can inhibit the binding of LDL to macrophages completely (96 and 100% inhibition, respectively), after cell surface heparin has been removed by treatment with heparinase. Using a solid-phase assay, we show that LDL binds specifically, saturably, and with high affinity to purified LRP (Kd = 5 nM). LDL can also completely inhibit the binding of alpha 2M* to purified LRP. These results indicate that LDL binds directly to LRP. The ability of LDL to cross-compete with alpha 2M* for binding to LRP suggests that LDL binds to a similar or overlapping site as alpha 2M*. In addition, the ability of alpha 2M* to inhibit most of the receptor-mediated binding of LDL to macrophages suggests that LDL receptors on murine peritoneal macrophages are predominantly LRP.

Animals↗
PubMed1991

DNA polymorphism haplotypes of the human lipoprotein lipase gene: possible association with high density lipoprotein levels.

Lipoprotein lipase (LPL) plays a central role in the metabolism of lipoproteins by hydrolyzing the core triglycerides of circulating very low density lipoproteins and chylomicrons. The enzyme is encoded by a gene about 30 kb in size located on the short arm of human chromosome 8. We have determined the locations of the four common DNA polymorphisms along the gene, including a polymorphism that occurred only among an American black population examined. These restriction site polymorphisms were used for haplotype analysis of Mediterranean and US black families. Estimation of the extent of nonrandom association between these polymorphisms indicated considerable linkage disequilibrium between these sites. No correlation was observed between the level of linkage disequilibrium and the physical distance of the polymorphic sites. The polymorphism information content of the haplotypes ranged from 0.65 to 0.74, thereby constituting a relatively useful genetic marker on chromosome 8. We tested for possible associations between the polymorphisms and circulating lipoprotein phenotypes in a population of 139 Caucasians undergoing coronary arteriography and 50 of their spouses. Some possibly significant associations between LPL gene polymorphisms and levels of high density lipoprotein cholesterol (P = 0.015) and total plasma cholesterol (P = 0.025) were observed. In contrast to a previous report, we found no significant associations with the levels of plasma triglycerides.

Adult↗
PubMed1989

Serum cholinesterase isoenzymes and the WHHL rabbit: the relationship between the activity of cholinesterase not bound to low-density-lipoprotein and lipoprotein titer.

Serum cholinesterase has been previously shown to complex with beta-lipoprotein in the plasma. Since serum cholinesterase exists as isoenzymes in plasma, the relationship between the activity of these isoenzymes (unbound to beta-lipoprotein) and lipoprotein titer was investigated. The results indicated that the total of C2, C3, and C4 isoenzyme activities were expressed within a narrow range and independent of low density lipoprotein titer. These findings may indicate that unbound plasma cholinesterase may undergo autoregulation independent of cholinesterase bound to beta-lipoprotein.

Animals↗
PubMed1984

Response of adipose tissue lipoprotein lipase activity and serum lipoproteins to acute hyperinsulinaemia in man.

In order to assess the short-term effects of hyperinsulinaemia and hyperglycaemia on adipose tissue lipoprotein lipase activity and on serum lipoproteins, we measured these variables in ten normal subjects during euglycaemic and hyperglycaemic hyperinsulinaemic clamps. The mean steady-state plasma glucose and insulin concentrations, respectively, were 4.7 mmol/l and 101 mU/l during euglycaemic moderate-insulin clamp, 4.9 mmol/l and 565 mU/l during euglycaemic high-insulin clamp, and 8.8 mmol/l and 148 mU/l during hyperglycaemic clamp. Saline infusion was used as control. The adipose tissue lipoprotein lipase activity rose significantly over 5 h during high-insulin clamp (p less than 0.01) and during hyperglycaemic clamp (p less than 0.05), but did not change during the moderate-insulin clamp. The magnitude of change of lipoprotein lipase activity from baseline (either rise or fall) was inversely related to the preclamp activity during euglycaemic moderate-insulin clamp (r = -0.67), during hyperglycaemic clamp (r = -0.68) and during infusion of saline (r = -0.75, p less than 0.05). Total serum triglyceride concentration decreased significantly during all clamp studies compared with the control experiment. This change was mainly accounted for by a decrease of VLDL triglyceride. The LDL cholesterol level fell by an average of 5% (p less than 0.05) during the high-insulin clamp and by 10% (p less than 0.05) during the hyperglycaemic clamp. The HDL cholesterol level did not change significantly. It is concluded that adipose tissue lipoprotein lipase activity in man is increased by physiological insulin levels during hyperglycaemia and also by supraphysiological insulin levels during euglycaemia, but is not influenced by physiological hyperinsulinaemia without hyperglycaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1990

Predictive value of lipoprotein (a) and other serum lipoproteins in the angiographic diagnosis of coronary artery disease.

To determine the relation among lipids in predicting coronary artery disease (CAD), 213 patients undergoing diagnostic angiography for suspected CAD were prospectively studied. Twenty-one patients had normal coronary arteries and 192 had CAD in 1 to 3 arteries at arteriography with measurements obtained with digital calipers. Lipoproteins were measured and lipoprotein (a) [Lp(a)] was also assayed in a subset of 98 patients with CAD. Statistical analysis was performed using uni- and multivariate techniques to test the association among age, gender, systemic hypertension, diabetes mellitus, cigarette smoking, family history, total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, very low density lipoprotein cholesterol, apolipoproteins (apo) A-I and apo B, ratio of apo A-I to apo B, and ratio of HDL cholesterol to total cholesterol, to Lp(a) and to CAD. All factors except gender, systemic hypertension, diabetes mellitus and cigarette smoking were univariate predictors of CAD. Multivariate predictors were, in decreasing order of significance, family history, age, HDL/total cholesterol ratio and apo B. When Lp(a) was included, multivariate predictors were age, family history, apo B and Lp(a), in that order. Lipid parameters alone showed that the HDL/total cholesterol ratio and that Lp(a) provide the best predictive tests for the detection of CAD in this referral population and may ultimately become important screening tests for CAD.

Coronary Angiography↗
PubMed1978

The effect of lipoprotein lipase and hepatic lipase on the electrophoretic mobility of lipoprotein-X.

Lipoprotein-X containing plasma from a patient with familial lecithin:cholesterol acyltransferase (LCAT) deficiency, was used as substrate and incubated with postheparin plasma or partly purified lipases. LP-X could not be demonstrated by agar gel electrophoresis after incubation with postheparin plasma from a healthy subject, from a patient with chronic active hepatitis deficient in hepatic lipase, or with partly purified lipoprotein lipase. After incubation a marked increase in free fatty acids (FFA) was observed. In contrast LP-X was still present after incubation when postheparin plasma deficient in lipoprotein lipase or partly purified hepatic lipase was added to the substrate. Only minor changes in the concentration of FFA occurred. After addition of oleic acid to the substrate LP-X could not be demonstrated by agar gel electrophoresis. However, in the isolated low density lipoproteins, LP-X like particles were still present as viewed by electron microscopy. Our results strongly suggest that the change in electrophoretic mobility of LP-X was induced by the release of FFA. This was achieved by lipoprotein lipase, but not by hepatic lipase.

Adult↗
PubMed1993

In vitro degradation of very low density lipoprotein from diabetic patients by lipoprotein lipase.

Fatty acid release by incubation with lipoprotein lipase (LPL) in vitro from very low density lipoproteins (VLDL) obtained from diabetic patients was low compared with that from healthy subjects, though the compositions were similar in both VLDL. Percentages of the large size VLDL decreased and those of the small size VLDL increased after the incubation with LPL. At the same time, on polyacrylamide gel disk electrophoresis, the smaller catabolic products from these VLDL appeared at a similar position to that of low density lipoproteins (LDL) and at the running front where high density lipoproteins (HDL) had migrated. The amount of the small size VLDL and the LDL-like lipoproteins produced from diabetic VLDL were less than those from normal VLDL and inversely correlated with the percent decrease of the large original size VLDL. This fact suggests that VLDL from diabetic patients are poor substrates for LPL compared with normal VLDL.

Diabetes Mellitus, Type 2↗
PubMed1984

The use of heparin-sepharose affinity chromatography to separate two distinct lipoproteins from the low density lipoprotein fraction of rat plasma.

Heparin-Sepharose affinity chromatography resolved rat lipoproteins isolated in the density range 1.019-1.063 g/ml into two distinct fractions. The first, which eluted with 150 mM NaCl, was shown by immunodiffusion and by polyacrylamide gel electrophoresis to contain predominantly apo E. On this basis the major lipoprotein present is identified as high density lipoprotein1 (HDL1). The second, eluted with 325 mM NaCl, contains predominantly apoprotein B by the same techniques. The main lipoprotein present is therefore identified as low density lipoprotein (LDL). The lipid composition of the two lipoproteins is similar. Both are rich in cholesterol ester, with a free to ester cholesterol ratio of about 1 to 2.5. From lipid and protein analyses on the two fractions, the plasma concentrations of HDL1 and LDL can be calculated to be about 14 and 12 mg/100 ml, respectively. Their mean diameters are 13 +/- 2 nm and 18 +/- 5 nm, respectively.

Animals↗
PubMed1987

Artery wall derived proteoglycan-plasma lipoprotein interaction: lipoprotein binding properties of extracted proteoglycans.

Artery proteoglycan-lipoprotein binding characteristics were determined using intact, high molecular weight chondroitin sulfate proteoglycans (CS-PG) isolated from grossly appearing normal aortas of atherosclerosis susceptible WC-2 pigeons and plasma lipoproteins from normolipemic, randomly bred White Carneau pigeons. Optimum formation of particulate proteoglycan-lipoprotein complexes occurred in 5 mM Tris, 6 mM KCl, 4 mM CaCl2, 1 mM MgSO4, pH 7.2. The binding of CS-PG was specific for low density lipoprotein (LDL) and not high density lipoprotein (HDL). The relative importance of the intact monomeric structure of the PG was suggested in studies where glycosaminoglycan chains isolated from the PG monomer possessed less than 1% of the binding reactivity of the intact PG. The core protein prepared from the CS-PG monomer formed no measurable particulate complex.

Animals↗